Adiponectin is an adipose-derived protein (adipocytokine) that is secreted by adipose tissue. It has insulin-sensitizing, anti-inflammatory and cardio-protective properties, and is thought to be protective against obesity-related diseases such as type 2 diabetes. Humans and cats are two species that commonly develop type 2 diabetes associated with insulin resistance, impaired beta cell function and spontaneous islet amyloid deposition. The domestic cat (Felis catus) has recently been proposed as an animal model for human type 2 diabetes. However, little is known about the physiology of adiponectin in cats. Therefore, we set out to investigate the association of adiponectin profiles with dietary carbohydrate intake, feeding, body weight, fat mass, and insulin sensitivity in healthy young adult cats (n=32; 2-4 years old; gender ratio 1:1; body condition 4-5/9). Cats were fed a moderate carbohydrate diet (37% ME) at maintenance energy requirements for four weeks. Cats were then assigned to either receive a low (19% ME) or high (52% ME) carbohydrate diet and fed at maintenance energy requirements for another four weeks, followed by ad-libitum feeding for eight weeks to facilitate weight gain. Adiponectin profiles including total circulating adiponectin and its distribution [low molecular weight (LMW) and high molecular weight (HMW) adiponectin], and proportion of adiponectin that is HMW (SA) were measured by ELISA and velocity sedimentation using sucrose gradients, followed by Western blotting, respectively. We demonstrated inter-animal variation in total adiponectin concentration at baseline (0.6 to 15.0 g/mL), with the adiponectin present in both LMW and HMW forms. Feeding with a high carbohydrate diet for four weeks at maintenance energy requirements resulted in increased total adiponectin concentration, which was associated with an increased concentration of LMW adiponectin. In contrast, feeding with a low carbohydrate diet for four weeks at maintenance energy requirements resulted in increased concentration of HMW adiponectin, decreased LMW adiponectin concentration, and increased SA, without a change in total adiponectin concentration. In cats fed the high carbohydrate diet, total adiponectin and HMW adiponectin concentrations become lower at six hours after feeding, as compared to the fasting concentrations. This phenomenon was not observed in cats fed a low carbohydrate diet, indicating a diet-dependent postprandial effect. There was no effect of gender on any of the adiponectin profiles in cats. Unlike other studies in humans and mice in which adiponectin concentrations decreased as fat mass increased, our data indicate that a moderate weight gain achieved by ad libitum feeding of a low carbohydrate diet for eight weeks correlated with increased adiponectin concentrations. Total adiponectin concentration (mirrored by HMW adiponectin) was positively correlated with body weight gain and fat mass gain (but not absolute fat mass) in our overweight cats. Furthermore, the fat mass-related increases in plasma adiponectin over eight weeks correlated with insulin sensitivity (higher adiponectin concentration corresponded to greater insulin sensitivity in overweight cats). These data hint at the possibility that in overweight animals, adiponectin is similar to other adipokines that rise concomitantly with increased of moderate fat mass gain and thus increases insulin sensitivity. Overall, the knowledge in this study therefore provides useful information to veterinarians and cat food manufacturers, and forms a foundation for future studies to extend our knowledge of adiponectin in cats. Data gathered in cats may also be applicable to humans and could therefore inform research using cats as an animal model of human obesity and type 2 diabetes.

Adiponectin is an adipose-derived protein (adipocytokine) that is secreted by adipose tissue. It has insulin-sensitizing, anti-inflammatory and cardio-protective properties, and is thought to be protective against obesity-related diseases such as type 2 diabetes. Humans and cats are two species that commonly develop type 2 diabetes associated with insulin resistance, impaired beta cell function and spontaneous islet amyloid deposition. The domestic cat (Felis catus) has recently been proposed as an animal model for human type 2 diabetes. However, little is known about the physiology of adiponectin in cats. Therefore, we set out to investigate the association of adiponectin profiles with dietary carbohydrate intake, feeding, body weight, fat mass, and insulin sensitivity in healthy young adult cats (n=32; 2-4 years old; gender ratio 1:1; body condition 4-5/9). Cats were fed a moderate carbohydrate diet (37% ME) at maintenance energy requirements for four weeks. Cats were then assigned to either receive a low (19% ME) or high (52% ME) carbohydrate diet and fed at maintenance energy requirements for another four weeks, followed by ad-libitum feeding for eight weeks to facilitate weight gain. Adiponectin profiles including total circulating adiponectin and its distribution [low molecular weight (LMW) and high molecular weight (HMW) adiponectin], and proportion of adiponectin that is HMW (SA) were measured by ELISA and velocity sedimentation using sucrose gradients, followed by Western blotting, respectively. We demonstrated inter-animal variation in total adiponectin concentration at baseline (0.6 to 15.0 g/mL), with the adiponectin present in both LMW and HMW forms. Feeding with a high carbohydrate diet for four weeks at maintenance energy requirements resulted in increased total adiponectin concentration, which was associated with an increased concentration of LMW adiponectin. In contrast, feeding with a low carbohydrate diet for four weeks at maintenance energy requirements resulted in increased concentration of HMW adiponectin, decreased LMW adiponectin concentration, and increased SA, without a change in total adiponectin concentration. In cats fed the high carbohydrate diet, total adiponectin and HMW adiponectin concentrations become lower at six hours after feeding, as compared to the fasting concentrations. This phenomenon was not observed in cats fed a low carbohydrate diet, indicating a diet-dependent postprandial effect. There was no effect of gender on any of the adiponectin profiles in cats. Unlike other studies in humans and mice in which adiponectin concentrations decreased as fat mass increased, our data indicate that a moderate weight gain achieved by ad libitum feeding of a low carbohydrate diet for eight weeks correlated with increased adiponectin concentrations. Total adiponectin concentration (mirrored by HMW adiponectin) was positively correlated with body weight gain and fat mass gain (but not absolute fat mass) in our overweight cats. Furthermore, the fat mass-related increases in plasma adiponectin over eight weeks correlated with insulin sensitivity (higher adiponectin concentration corresponded to greater insulin sensitivity in overweight cats). These data hint at the possibility that in overweight animals, adiponectin is similar to other adipokines that rise concomitantly with increased of moderate fat mass gain and thus increases insulin sensitivity. Overall, the knowledge in this study therefore provides useful information to veterinarians and cat food manufacturers, and forms a foundation for future studies to extend our knowledge of adiponectin in cats. Data gathered in cats may also be applicable to humans and could therefore inform research using cats as an animal model of human obesity and type 2 diabetes.